The long-term objectives of this project are to elucidate the neural and hormonal bases of learned vocal behavior in passerine birds. Birds must hear an external auditory model during a restricted period of development in order to subsequently form an accurate vocal copy of that pattern. Exposure to conspecific vocal sounds beyond this "sensitive period" is of little or no value for vocal learning. We have previously provided evidence for additional, separate sensitive periods during vocal development. For example, lesions of a specific neural circuit disrupt vocal behavior in young birds during vocal learning, but have no effect on song production in older juveniles and adults. Thus, there is a "learning circuit" in the forebrain that is involved with vocal development during a restricted period, but not with subsequent maintenance of stereotyped vocal patterns. In addition, we have shown that there are also sensitive periods when circulating hormone levels must be at specific levels in order for vocal learning to develop normally. We would like to investigate the factors that regulate these and other sensitive periods during vocal learning in order to begin to elucidate the cellular mechanisms by which organisms learn to communicate vocally. Experiments to be conducted include the following: (1) Does blocking the action of hormones extend the sensitive period for the effect of lesions in the learning circuit of the forebrain? (2) What are the exact times during development when altered hormone levels (either too high or too low, respectively) disrupt vocal learning? We anticipate that periods requiring low vs. high hormone levels may be non-overlapping, and correlate with distinct aspects of vocal learning. (3) We will selectively lesion different levels of the learning circuit as well as brain regions known to be important for adult vocal production at different times during vocal development in order to assess their contribution to behavior at different stages of learning. (4) Lesions at one level of the learning circuit induce neuronal death in adjacent levels of this circuit only in juvenile birds during vocal learning, but not in adults. We will begin to investigate the role of target factors and afferent inputs in this induced cell death during vocal learning. (5) Neurogenesis continues throughout the life span in songbirds, and new neurons are incorporated into neural circuits for vocal learning at an enhanced rate during song development. We will determine whether this neuronal addition is due to enhanced cellular proliferation in the forebrain during vocal development. (6) We will determine whether there is a sensitive period for reliance on auditory feedback of self-produced vocalizations during vocal development. These experiments will bear importantly on hypotheses for neural and endocrine mechanisms of vocal learning in humans, and may have important implications for problems of vocal perception and production in humans such as stuttering and dyslexia.